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Fatty liver and drugs: the two sides of the same coin.
Miele, L; Liguori, A; Marrone, G; Biolato, M; Araneo, C; Vaccaro, F G; Gasbarrini, A; Grieco, A.
Afiliação
  • Miele L; Institute of Internal Medicine and Gastroenterology Area, Fondazione Policlinico Universitario A. Gemelli, Catholic University of the Sacred Heart, Rome, Italy. luca.miele@policlinicogemelli.it.
Eur Rev Med Pharmacol Sci ; 21(1 Suppl): 86-94, 2017 03.
Article em En | MEDLINE | ID: mdl-28379591
ABSTRACT
Drug-induced liver injury (DILI) is a common and underestimated cause of liver disease. Several drugs and other xenobiotics can be the cause of different clinicopathologic patterns of liver disease. Steatosis and steatohepatitis are rare but well-documented types of DILI. Over the past decades commonly used drugs like amiodarone, tamoxifen, irinotecan, methotrexate, valproic acid and glucocorticoids have been recognized to be associated with steatosis. Even though the pathophysiological pathways are still only partially understood, inhibition of mitochondrial beta-oxidation, reduced very low-density lipoprotein secretion, insulin resistance induction and increased de novo synthesis or increased liver uptake of fatty acids are considered the main pathogenic mechanisms through which drugs can lead to hepatic steatosis. On the other hand, fatty liver itself is a very common clinical condition, and there is a growing awareness of the potential risk factors for DILI due to the underlying metabolic condition itself.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fígado Gorduroso / Doença Hepática Induzida por Substâncias e Drogas Tipo de estudo: Risk_factors_studies Limite: Humans Idioma: En Revista: Eur Rev Med Pharmacol Sci Ano de publicação: 2017 Tipo de documento: Article
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Fígado Gorduroso / Doença Hepática Induzida por Substâncias e Drogas Tipo de estudo: Risk_factors_studies Limite: Humans Idioma: En Revista: Eur Rev Med Pharmacol Sci Ano de publicação: 2017 Tipo de documento: Article